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Pharmacology · Neuromuscular blockers: interaction with aminoglycosides
Sample itemA 55-year-old man undergoing bowel surgery receives vecuronium. Intraperitoneal gentamicin lavage is used at the end, and he remains weak and poorly ventilated, with fade on train-of-four stimulation although neostigmine has been given. Which mechanism best explains the prolonged block?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Aminoglycosides reduce presynaptic acetylcholine release and postjunctional sensitivity, adding to the block
Aminoglycosides interfere with calcium-dependent acetylcholine release and decrease the sensitivity of the motor endplate, so they potentiate non-depolarising blockers and can resist reversal. Magnesium, volatile anaesthetics and calcium channel blockers have similar additive effects. Management is supportive ventilation with calcium and further reversal, such as sugammadex for aminosteroid blockers.
Option by option
A. Gentamicin inhibits plasma cholinesterase and so delays vecuronium breakdown
Vecuronium is eliminated by the liver and kidney, not by plasma cholinesterase, which gentamicin does not inhibit.
B. Aminoglycosides reduce presynaptic acetylcholine release and postjunctional sensitivity, adding to the block (correct)
Reduced presynaptic release and postjunctional sensitivity add to competitive blockade at the endplate.
C. Gentamicin induces hepatic enzymes that convert vecuronium to an active metabolite
Vecuronium is not converted to a more active metabolite through enzyme induction by gentamicin.
D. Gentamicin displaces vecuronium from plasma proteins
Protein-binding displacement does not explain a persistent block of this kind and gentamicin is not a binding competitor.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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